Published: July 23, 2020
Oral immunotherapy (OIT) aims to establish desensitization and sustained unresponsiveness (SU) to specific allergens in food allergy patients, but little is known about the mechanisms by which OIT induces SU.
In a research article recently published in The Journal of Allergy & Clinical Immunology (JACI), Yoneyama and colleagues investigated the cells and molecules involved in the establishment of SU by OIT using a mouse model of OIT. The authors hypothesized that Notch receptor-mediated signaling, which regulates the differentiation of various immune cells, might be involved in the establishment of SU, and to test this hypothesis, they administered a Notch signaling inhibitor to the mouse model during OIT treatment period.
Administration of a Notch signaling inhibitor to the mice disrupted the establishment of SU, but did not affect the induction of desensitization. OIT resulted in a systemic expansion of Th2 cells producing both IL-4 and IL-10 and myeloid-derived suppressor cells, but the expansion was suppressed by inhibition of Notch signaling.
Notch signaling contributes to the establishment of SU through systemic expansion of the immunosuppressive cells. These findings provide insights into how patients with food allergies can achieve SU by OIT. In addition, the frequencies of Th2 cells producing both IL-4 and IL-10 and myeloid-derived suppressor cells may be markers of whether OIT can be successfully completed.
The Journal of Allergy and Clinical Immunology (JACI) is an official scientific journal of the AAAAI, and is the most-cited journal in the field of allergy and clinical immunology.